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Focus on CME at the
University of Toronto
It was previously thought that erectile dysfunction (ED) was essentially a
psychologic disorder. Increasingly, however, sophisticated medical
examinations are now able to determine physical causes for ED.
By Magdy M. Hassouna, PhD, MD, FRCPC
rectile dysfunction (ED) is defined as the
inability to achieve or maintain an erection
sufficient for satisfactory sexual function.1 It was
previously thought that ED was essentially a psychologic disorder. Recently, however, the majority
of men with ED have been found to have an under-
Dr. Hassouna is associate professor of surgery
(urology), University of Toronto, and urologist,
The Toronto Hospital — Western Division, Ontario.
lying organic cause.2 ED also encompasses disorders in ejaculation and orgasm.
How Common Is It?
Kinsey et al reported the results of a survey conducted on 15,781 men. The survey suggested that
the prevalence of ED was less than 1% in men
under age 30, 6.7% in men between the ages of
45 to 55, and 25% in men above 65 years.3
The Massachusetts Male Aging Study (MMAS)
was a cross-sectional community-based randomsample survey in men aged 40 to 70. The study was
conducted between 1987 and 1989 in 11 cities
around Boston. Although the sample population
The Canadian Journal of CME / November 2001 211
Erectile Dysfunction
Erection Theories of Yesteryear
Many theories have
attempted to explain the
erectile process. The
presence of intravascular
protrusions (i.e., pollsters)
was first proposed in
1869.7 It was postulated
that an erection was the
result of active
contraction and
relaxation of these
“cushions” or
protrusions in
the afferent and
efferent penile vasculature,
and that tumescence was
produced by the shunting of
arterial blood to cavernous
spaces as a result of the
concomitant relaxation of
arterial pollsters and the
contraction of the venous
pollsters. In more detailed
animal studies and in studies
on young human males, Newman et al did
not find any pollsters, and suggested that
pollsters may represent a response to
was less than the cohort in Kinsey’s study, the
MMAS addressed several pertinent questions
related to sexuality in aging men.4 The study
showed that the prevalence of ED in this population was 52%. The projected number of men
who will be affected by ED for the year 2005 is
more than 50 million men between the ages of
40 and 70.5
212 The Canadian Journal of CME / November 2001
Another study showed evidence that the
prevalence of ED was significantly associated
with age (p < 0.001), and correlated with a lower
quality of life (P < 0.001).6
Mechanisms of Erection
Neuroanatomy. The neural mechanisms
responsible for erections in men are still poorly understood. It is known, however, that
there are two kinds of penile erections:
reflexogenic and psychogenic.
Peripherally, the penis is innervated by both
divisions of the autonomic nervous system, as
well as the somatic sensory nerves through the
pudendal nerve. The pudenal nerve arises from
the S2-S4 segments of the spinal cord in Onuf’s
nucleus, and supplies the skin of the dorsal, and
the lateral aspects of the shaft and the glans.
Other sensory contribution comes from the
ilioinguinal nerve; this nerve particularly affects
the skin of the ventral base of the penis and the
anterior part of the scrotum. The parasympathetic innervation to the penis originates as preganglionic fibers from the intermediolateral
nuclei in the S2-S4 spinal segments. Nerve
fibers form a plexus that courses laterally in the
endopelvic fascia close to the hypogastric vessels, terminating beside the rectum into the
pelvic plexus. Branches from the plexus innervate the urinary bladder, lower ureter, seminal
vesicles, prostate, rectum and urethra.
Two critical branches (called the cavernous
nerves) have been implicated in the mechanisms
of erection. The cavernous nerves travel along
the posterolateral aspects of the prostate to the
corpora cavernosa. At the base of the prostate,
the cavernous nerves are located lateral to the
capsule of the prostate. Distally, the cavernous
nerves are at the five and seven o’clock position
near the apex of the prostate. The sympathetic
innervation of the penis is derived from the tho-
Erectile Dysfunction
racolumbar portion of the spinal cord (specifically T11-L2). The efferent fibers run through
the retroperitoneum towards the hypogastric
plexus. These nerves contribute to the pelvic
plexus and the cavernous nerves, and are responsible for emission and ejaculation.
The arterial supply of the penis is derived
from the internal pudendal artery. This artery
branches from the ischiopudendal trunk of the
internal iliac artery, which contributes to the
vascular supply of the prostate.
Hemodynamics of Erection
The past decade had witnessed a surge in the
understanding of the physiology of erection. This
knowledge has tremendously aided researchers
who are investigating methods to treat ED, and
has helped design some treatment options, particularly vasoactive drugs.
Extensive investigations in animal models9 and
human volunteers10 have settled some of the controversy regarding the mechanism of erection (see
sidebar). During erection, there is an increase in
arterial blood-flow, sinusoidal relaxation and
venous resistance, resulting in turgidity of the corpora cavernosa and corpus spongiosum (i.e., vascular or full-erection phase). Subsequent contraction of the bulbocavernosus and ischiocavernosus
muscles either spontaneously or reflexively compresses the proximal corpora, culminating in cavernosal rigidity and further engorgement of the
glans penis; this is commonly seen during masturbation or intercourse (i.e., skeletal muscle or rigiderection phase). In full erection, the pressure in the
corpora cavernosa is approximately 90 mmHg to
100 mmHg, while the pressure in the glans penis
is 40 mmHg to 50 mmHg. In the rigid-erection
phase, compression of the blood-distended corpora can increase the intracavernous pressure well
above the systolic pressure.11
In the flaccid state, the arterioles are constricted
and the sinusoids are contracted; together, they exert
maximum resistance against arterial flow, allowing
only a small amount of blood to enter the corpora for
nutritional purposes. The venules in the periphery of
the corpora run between the corpora and the adjacent sinusoidal wall, while the larger intermediary
venules run between the sinusoidal wall and the
tunica albuginea for some distance before exiting as
the emissary veins. When the sinusoids are contracted (in the flaccid state), these venules drain freely to
the extra penile veins. During erection, the smooth
muscles of the sinusoids and arterioles relax,
increasing sinusoidal compliance and causing
peripheral resistance to decrease to a minimum; this
Intensive investigations have
settled some of the controversy
regarding the mechanism of
erection. During erection, there is
an increase in arterial blood-flow,
sinusoidal relaxation and venous
results in a sudden increase in the arterial flow, dilation of the arterial tree and a filling of the sinusoids.
Dilation of the arterial tree allows blood to rush in,
and permits transmission of about 80% of the systolic pressure to the sinusoidal spaces. This high
intracavernous pressure converts a soft flaccid organ
to a blood-distended erect penis.11,12
Distension of the sinusoids within a limited space
(because of a relatively indistendable tunica albuginea) results in a compression of the small venules
between the sinusoids. Further expansion of the
sinusoids during full erection compresses the intermediary venules between the sinusoidal wall and the
The Canadian Journal of CME / November 2001 213
Erectile Dysfunction
Pudendal arterial
flow (mL/min)
Intracorporeal pressure
(cm H2O)
Cavernous Nerve
Pudendal Nerve
Figure 1. Arterial blood flow and intracavernous pressure changes during the different phases of penile erection in experimental animals
tunica albuginea. Stretching of the tunica albuginea
also compresses the emissary veins. These actions
reduce the venous capacity to a minimum, efficiently obtaining and maintaining erection in the corpora
cavernosa without diverting too much cardiac output for penile erection. In contrast, the glans penis
(with no tunica albuginea) remains flaccid during
the erection.
214 The Canadian Journal of CME / November 2001
The Six Phases
of Penile Erection
Based on the actions of the arterial, venous and
sinusoidal systems, Lue et al described six phases
of penile erection (Figure 1).11,12
Flaccid phase. In the flaccid state, only a minimal amount of blood flow enters the corpora cav-
Erectile Dysfunction
ernosa for nutritional purposes. The pH, PCO2 and
PO2 of blood from the corpora cavernosa are at levels maintained in venous blood. High-resolution
ultrasound and doppler study in humans show that
the paired cavernous arteries at the base of the penis
have an average inner diameter of 0.05 cm. Peak
velocity of blood flow is usually 15 cm/second, or is
not detectable.
Latent (filling) phase. There is increased blood
flow in the internal pudendal artery during both the
systolic and the diastolic phases, without an increase
in intracavernous pressure. The penis shows slight
elongation and fullness. The highest blood-flow rate
occurs during this phase, with a peak flow velocity
over 30 cm/second and a two-fold dilation of the
cavernous arteries.
Tumescence phase. The penis rapidly expands
and elongates to its maximum capacity. The intracavernous pressure continues to increase, and, subsequently, blood inflow decreases.
Full-erection phase. During this phase, the intracavernous pressure can rise to as much as 85% of
the systolic pressure, and becomes more steady.
Blood flow in the internal pudendal artery is less
than the blood flow during the tumescence phase.
Although the venous channels are mostly compressed, the venous flow is slightly higher than what
it is during the flaccid state, and blood gases of the
intracavernous blood are maintained at the same
level as in the arterial side.
Skeletal or rigid-erection phase. As a result of
the contraction of the ischiocavernosus muscles, the
intracavernous pressure rises well above the systolic
pressure, causing rigid erection. During this phase,
there is almost no blood flow through the cavernous
artery. The short duration of this phase, however,
prevents the development of ischemia.
Detumescence phase. After ejaculation or the
cessation of erotic stimuli, sympathetic tonic discharge resumes, resulting in the contraction of the
smooth muscles around the sinusoids and arterioles.
The blood flow diminishes to the level it had during the flaccid phase, and a large portion of blood is
expelled from the sinusoidal spaces. The penis
returns to its flaccid length and girth.
Why Erectile Dysfunction?
Penile erection is a complex physiologic
response that is dependent on the integration of
psychogenic, endocrine, vascular and neurogenic mechanisms. Disturbance of one or more
of these mechanisms will result in erectile dys-
Men with primary psychogenic
impotence often come from
sexually repressed backgrounds,
where sex
was not discussed or was treated
as sinful and immoral.
function. The individual causes are many, and
each cause may work by more than one mechanism (e.g., diabetes mellitus can cause ED
through vascular and neurologic causes).
Additionally, several mechanisms or causes may
work simultaneously in a cumulative fashion to
produce severe erectile dysfunction. The reported incidence of impotence varies with age,
affecting 5% of men who are 40 to 49 years old,
and 85% of 80-year-old men.13
Psychogenic Factors:
How Important are They?
In the past, psychogenic factors were considered
to be very important in causing ED; more than
90% of impotent patients were diagnosed to be
psychogenic.14 Increasingly, sophisticated medThe Canadian Journal of CME / November 2001 215
Erectile Dysfunction
ical examinations are now able to determine
physical causes for dysfunctions that, in the past,
would have been diagnosed as having a psychogenic base. In a systematic, multidisciplinary, multidimensional assessment of a large
number of impotent men, an organic cause was
found in 35.9% of men, a psychogenic cause was
found in 38.3%, and multiple or indeterminate
causes in 28.8% of men.15
Men with primary psychogenic impotence
often come from sexually repressed backgrounds, where sex was not discussed or was
treated as sinful and immoral. Generally, anxiety
and depression are believed to be the major
causes of psychogenic sexual dysfunction. These
The prevalence of endocrine
disorders in a population of
impotent men is estimated to be
between 5%
and 35%.
emotions may be the result of nonsexual concerns, or may be specific to the sexual situation.
The presence of anxiety and depression may be
a result of impotence, as well as a precipitating
factor for ED.16 It must be stressed that identifying a possible psychologic factor does not mean
that this factor is the sole cause of impotence.
Psychologic evaluation is important in both
the diagnosis and treatment of sexual dysfunction. The interview and the questionnaire are two
tools typically used for this evaluation. It is
helpful to interview the couple together as well
as apart, in case there is information one would
rather not share with the other.16 Some studies
have shown that interviewing the partner of the
216 The Canadian Journal of CME / November 2001
individual with ED confirmed the diagnosis in
82% of cases, and changed the diagnosis in 18%
of the cases. Studies regarding the partner’s
impact on treatment showed that in 42% of the
cases, there was no change in the chosen treatment modality, in 18% of the cases, there was a
change of treatment due to a change in diagnosis
and in 40% of the cases, there was a change in
the chosen treatment modality, even though the
diagnosis was confirmed.17
The Endocrine Factor
The prevalence of endocrine disorders in a population of impotent men is not clear, but is estimated to be between 5% and 35%.18 Many hormones
may affect sexual performance, but androgens and
prolactin play the most important role.19
Testosterone, the principal androgen in the
male, is secreted primarily by the testicular Leydig
cells. The adrenals also secrete some testosterone.
Testosterone secreted by Leydig cells is regulated
by the hypothalamus and the pituitary gland
through the hypothalamic pituitary gonadal axis.
Testosterone affects its target tissues either directly or after it has been intracellularly converted to
dihydrotestosterone (DHT). Although the effects
of both androgens (testosterone and DHT) are well
established, their role and the level required for
normal erectile physiology and sexual behavior
are still being investigated.20
Some studies have demonstrated that castrated
and hypogonadal men were able to maintain sexual
activity. It was found that androgen replacement in
hypogonadal individuals had a significant effect on
sexual behavior and activity that was dosedependent, and could not be reproduced by placebo.
Hypogonadal men who received an androgen
replacement experienced a return of libido, mood
elevation and restoration of ejaculation. For men
with erectile potency, the situation is more complex. It appears that the physiologic capacity for
Erectile Dysfunction
erection is less sensitive to androgen withdrawal
than are sexual interest and sexual activity.
Androgen-dependent spontaneous erection (diurnal
and nocturnal) is markedly suppressed in hypogonadism, and is restored by androgen replacement.
In contrast, erections in response to erotic films are
unaffected by androgen replacement, despite the
marked effects of androgen on sexual interest and
behavior. The central process leading to spontaneous erections is androgen-dependent, whereas the
mechanism leading to erection in response to a certain type of external erotic stimuli remains intact
despite androgen deficiency. Although the
importance of androgens for normal sexual
interest and activity has been established, the
amount of androgens required for both basal and
optimal function is still unknown, and may have
vary by individual. Not only may the circulating
level of testosterone be important, but there may
also be more basic physiologic mechanisms
working at the molecular level (i.e., receptor site
Prolactin has a complex relationship with
gonadotropins. In men with hyperprolactinemia
and testosterone deficiency, serum Luteinizing
hormone (LH) levels are inappropriately low,
indicating the failure of the hypothalamic pituitary axis to respond to a reduced amount of
testosterone. Prolactin also appears to inhibit
gonadotropin-releasing hormone (GnRH).
Individuals with prolactin-secreting tumors
respond to an infusion of GnRH by increasing
the level of LH. In addition, GnRH may have a
direct effect on the central nervous system.
Some of the most common causes of hyperprolactinemia include pituitary tumors, primary
hypothyriodism and drug-related and idiopathic
Abnormalities in the thyroid hormone may
alter the hypothalamic pituitary gonadal axis,
resulting in ED. Hypothyroidism causes both
Erection is essentially a
hemodynamic process; vascular
diseases are, therefore, the
leading causes of erectile
dysfunction. In the majority of
cases, intervention is successful.
an increase in the estradiol production rate and
a decrease in its metabolic clearance, resulting
in an elevation of serum estradiol. The Leydig
cells may be inhibited by the high estradiol levels and/or by circulating antibodies to thyroidstimulating hormone. The decreased libido seen
in patients with hyperthyroidism may be due to
the hypermetabolic effects of thyroxine or the
increased level of circulating estrogen. 23
Individuals with hyperthyroidism also comThe Canadian Journal of CME / November 2001 217
Erectile Dysfunction
plain of sexual dysfunction. In these patients,
testosterone secretion is decreased, and the
metabolic transformation of testosterone shifts
towards etiocholanolone rather than androsterone. The elevated serum prolactin levels in
individuals with primary hypothyroidism
(mediated by the feedback-induced thyrotropin-releasing hormone [TRH]) may also
contribute to impotence.
The incidence of decreased libido and potency
in acromegalic individuals with elevated levels of
growth hormone is as high as 50%, due to hypothalamic pituitary dysfunction and increased
serum prolactin.21
mellitus, blunt perineal or pelvic trauma and
pelvic irradiation.24
Veno-occlusive disorders or venogenic impotence could be defined as occurring when the
penile arterial inflow is less than venous outflow. When tests such as dynamic infusion cavernosometry and cavernosography are performed on men with vasculogenic impotence,
about 55% to 88% of the men are found to have
a venous leak. For practical purposes, however,
venogenic impotence could be defined as occurring only when excessive venous outflow prevents full erection in the presence of normal
arterial blood flow.25
Peripheral Vascular Disease:
A Leading Cause of ED
Neurologic Factors
Erection is essentially a hemodynamic process;
vascular diseases are therefore the leading causes of erectile dysfunction. In the majority of
cases, intervention is successful. Alteration in
the flow of blood to (arterial) and from (venous)
the penis are the two mechanisms by which vascular impotence occurs. Decreased arterial flow
to the penis may be due to various causes. The
most well known cause is Leriche’s syndrome,
or thrombotic obliteration of the aortic bifurcation, with resultant pain and claudication of the
hips and thighs, and, in males, impotence.
Atherosclerotic and traumatic arterial occlusive
diseases of the hypogastric cavernous arterial
bed can decrease the perfusion pressure and the
arterial flow to the lacunar spaces, thus decreasing the rigidity of the erect penis and increasing
the time to maximal erection. Fibrosis, calcification and obliteration of the small cavernous vessels (which may occur with aging) have the same
effect. Common risk factors associated with
arterial insufficiency include hypertension,
hyperlipedemia, cigarette smoking, diabetes
218 The Canadian Journal of CME / November 2001
Neurologic impotence is said to exist if a neuropathic process (either central or peripheral)
results in failure to initiate the arteriolar and
lacunar smooth-muscle relaxation that facilitates
the hemodynamic alteration associated with
penile erection. Neurogenic factors have been
estimated to be the sole or major contributing factor in 10% to 20% of all organically impotent men.
The pelvic cavernous nerve complex is the major
pathway for neurologic control of penile erection.
Impairment of this pathway or other neurologic
pathways that utilize the pelvic cavernous nerve as
the final common pathway will result in neurogenic impotence. These pathways include the dorsal-nerve afferent pathway (both peripherally and
centrally), as well as the poorly described efferent
Neurologic causes of impotence are most commonly peripheral neuropathy, spinal-cord lesions
or lesions of the cerebral hemisphere. Peripheral
neuropathy may result from a variety of causes;
the most important cause is diabetes mellitus.
Patients with chronic renal failure (particularly
those undergoing hemodialysis) are frequently
impotent. Even though uremic neuropathy may
Erectile Dysfunction
contribute to impotence through Schwan’s cell
dysfunction, the hormonal abnormalities associated with uremia are most likely the primary cause.
Amyloidosis, with involvement of the autonomic
nervous system, can cause neurogenic impotence,
especially the familial type. Multiple sclerosis is
characterized by a loss of myelin in the white matter of the brain, brain stem and spinal cord. The
impact of MS on potency is variable, affecting
35% to 43% of MS patients The severity of impotence is directly related to the duration of the disease, but in several patients, sexual potency tended to remit and relapse. Other causes of spinalcord lesions that can affect potency include those
accompanying syphilis (tabes dorsalis), spina bifida,
syringomyelia, amyotrophic lateral sclerosis and
compression from a herniated disk or tumor.
Diabetes Mellitus (DM)
and Erectile Function
The prevalence of erectile dysfunction in men
with DM ranges from 35% to 75%, and is two to
five times higher than the prevalence of ED in
healthy control subjects. ED occurs 10 to 15 years
earlier in diabetic patients than in nondiabetic
ones, and is often an early complication of DM.
Some studies report that impotence may often be
the only symptom that leads to the discovery of
unrecognized DM.27
Evaluation for Erectile
History and physical examination. When taking a
patient’s history, the physician should emphasize the
following issues (Table 1):
1. Duration of the ED. An onset of short duration
should always point to the possibility of a psychogenic background. The lack of nocturnal and
Table 1
Evaluation of Erectile Dysfunction
• Sexual function questionnaire
• Gatrointestinal disease or surgery
• Pelvic or spinal trauma
• Vascular or endocrine diseases
• Neurologic diseases
• Sleep disorders
• Marital and sexual history
• Medications
• Tobacco and alcohol consumption
morning erection signals a more organic cause for
the ED. The patient should be asked to describe the
problem in his terms: Is it consistent with the same
sexual partner or does it vary if more than one partner is involved? The patient should also be encouraged to relate the frequency of the problem and the
frequency of sexual encounters that were not satisfactory. One should also ask the patient about his
libido and sexual gratification during the orgasm.
2. Circumstances surrounding the ED. The subtle
onset of ED should always point to the possibility of
an organic cause. Physicians should inquire about
any changes in the general health of the patient to
rule out an associated disease.
3. Medical history. Special interest should
always be paid to the medication the patient is
taking. The majority of antihypertensive drugs
are associated with variable degrees of ED.
Antipsychotic drugs are also associated with
ejaculation disorders, particularly delayed ejaculation and lack of libido. The patient should
The Canadian Journal of CME / November 2001 219
Erectile Dysfunction
understand that he should not voluntarily interrupt the treatment because of any side effects he
may experience. Every effort should be made to
substitute the offending drug with another drug
that has fewer side effects.
As previously mentioned, diabetes mellitus is
associated with ED.
4. Surgical history. ED usually occurs following extensive pelvic surgery. Radical prostatectomy is notoriously associated with ED in more
than 50% of cases. Other pelvic surgeries
(e.g., abdomino-perineal resection of the rectum,
surgery of the retroperitoneum, extensive fracture for the pelvic girdle) are known to cause ED.
With a better understanding of the
mechanisms of hemodynamics
involved in erection, several
different methods have been
proposed to help restore penile
In the physical examination, physicians
should emphasize the general habitus and the
degree of masculinization of the patient (such as
secondary sexual characteristics [e.g., pubic
hair, gynecomastia]) as part of the evaluation of
the endocrinal status.
Local examination involves an estimation of
the consistency, size and location of the testes,
looking for any possible anomalies. The penile
size and any abnormal fibrosis should be documented. Occasionally, a Polaroid ® picture
depicting the penis in an erect state is a very
effective method to assess the degree of curvature for future reference.
220 The Canadian Journal of CME / November 2001
What Specific Tests Should
Be Performed?
Laboratory tests are needed only if the diagnosis
of hypogonadism cannot be confirmed during the
history and the physical examination. These tests
should not be ordered indiscriminantly, since they
have not been proven to be cost-effective.
Specific tests should be requested if the diagnosis is unclear or if the patient requests a full investigation for a litigation problem.
Color duplex Doppler penile ultrasound is a relatively noninvasive test that can detect changes in
the arterial and venous penile blood flow. When
performed in conjunction with the intracavernosal
injection of a vasoactive agent, this test helps predict the patient response to local therapy.
Diurnal penile tumescence has gained popularity because of its simplicity and reproducibility.
This test involves the study of the erection and
rigidity by a Rigiscan® under erotic visual stimulation.
Cavernosometry-caverosography should be
performed to diagnose the possibility of a venoocclusive disease. Currently, these tests are not
commonly ordered, due to their invasiveness and
poor yield.
Penile electrophysiologic studies such as conduction velocity and cortical-evoked potentials are
very sophisticated tests used to uncover any
changes in the penile innervation in patients with
peripheral neuropathy. These studies are also helpful in medico-legal cases to document any subtle
damage to the penile innervation.
Pudendal arteriography is usually reserved for
patients with localized arterial blockage, and is
often performed prior to surgical arterialization of
the penis.
Office injection of a vasoactive drug in a cumulative dose is a very cost-efficient method of
assessing the patient’s response. A full rigid erec-
Erectile Dysfunction
tion after 10 to 15 minutes and lasting 30 minutes is
indicative of a vascular disorder that is not major.28
Treatment of Erectile
The treatment of ED has taken a major turn during the last two decades. With a better understanding of the mechanisms of hemodynamics
involved in erection, several different methods
have been proposed to help restore penile erection.
Vasoactive local drugs. The principle behind
the application of vasoactive drugs is to induce a
sudden decrease in the vascular resistance in the
cavernous bodies. The resulting sinusoidal
relaxation will enable blood to pool in the corpora cavernosa to induce rigidity.
For practical purposes, there are three drugs
available that can be used alone or in combination:
prostaglandin E1 PGE1.
After the basic examination and tests have
been conducted, intracavernosal administration
of these drugs should be presented to the patient
as a treatment option. The patient should be
made aware of the limitations, side effects and
long-term complications of this therapy. The
recently introduced intraurethral-installed PGE1
(Muse®) has been embraced for its simplicity in
delivering the drug. The price and the inconsistency of response are the main drawbacks of the
Vacuum constriction device. The principle
behind this device is to create a vacuum around
the penis using a specially designed cylinder,
resulting in blood pooling in the corpora cavernosa. An elastic band is applied around the base
of the penis to maintain the rigidity. Proponents
of this device praise its simplicity and efficiency.
Complications are usually minor, in the form of
local bruising. Use of this device necessitates
patient education and support.29
Systemic oral drugs. The presence of sildenafil has changed the way ED is treated.
Sildenafil is a potent inhibitor to cyclic GMP,
and therefore increases the penile response to
sexual stimulation. There have been several
studies confirming the efficacy and safety of
sildenafil in patients with variable etiologies of
The main side effects of sildenafil are
headache, flushing, dyspepsia and visual disturbances.
Surgical treatment. The demand for surgical
implantation of a penile prosthesis has declined
in the recent years with the introduction of less
invasive and efficient ways of restoring erection.
Penile implants can be divided into two general
types: nonhydraulic (semirigid) and hydraulic.
The surgical principle is to dilate the cavernous
tissue and to replace it with two cylinders of adequate length and girth. The surgery is invasive
and carries a risk of complications. The patient
should understand the limitations and the possible complications of penile implants.
Management of ED should include a proper
evaluation of the patient’s symptoms. Special
investigation tests should be tailored to the individual patient’s needs. Invasive tests should be
reserved according to the patient’s desire, and in
medicolegal cases. In the majority of cases,
treating the underlying cause of ED is not practical or feasible. The treating physician should
discuss the different treatment options with the
patient and provide the treatment that is acceptable to the patient. CME
The Canadian Journal of CME / November 2001 221
Erectile Dysfunction
1. NIH Consensus Development Panel on Impotence: NIH
Consensus Conference on Impotence. JAMA 1993;
2. Foreman MM, Doherty PC: Experimental approaches to
the development of pharmacological therapies for erectile
dysfunction. In: Riley A, M Peet M, Wilson C (eds).
Sexual Pharmacology. Oxford, Oxford Medical
Publications, 1993, p. 87-113.
3. Kinsey AC, Pomeroy WB, Martin CE: Sexual behaviour
in the human male. W.B. Saunders, Philadelphia, 1948.
4. Feldman HA, Goldstein I, Hatzichristou D, et al:
Impotence and its medical and psychological correlates:
Results of the Massachusetts Male Aging Study. J Urol
1994; 151(1):54.
5. United States Bureau of the Census: Statistical Abstract
of the United States 1992, 112th ed. Washington, DC,
6. Jonler M, Moon T, Brannan W, et al: The effect of age,
ethnicity and geographical location on impotence and
quality of life. Br J Urol 1995; 75(5):651.
7. Aboseif SR, Lue TF: Hemodynamics of penile erection.
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